Open AccessNeuronal Induction of Bone‐Fat Imbalance through Osteocyte Neuropeptide Y
Author(s) -
Zhang Yan,
Chen ChunYuan,
Liu YiWei,
Rao ShanShan,
Tan YiJuan,
Qian YuXuan,
Xia Kun,
Huang Jie,
Liu XiXi,
Hong ChunGu,
Yin Hao,
Cao Jia,
Feng ShiKai,
He ZeHui,
Li YouYou,
Luo ZhongWei,
Wu Ben,
Yan ZiQi,
Chen TuanHui,
Chen MengLu,
Wang YiYi,
Wang ZhenXing,
Liu ZhengZhao,
Luo MingJie,
Hu XiongKe,
Jin Ling,
Wan TengFei,
Yue Tao,
Tang SiYuan,
Xie Hui
Publication year - 2021
Publication title -
advanced science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.388
H-Index - 100
ISSN - 2198-3844
DOI - 10.1002/advs.202100808
Subject(s) - osteocyte , endocrinology , neuropeptide y receptor , medicine , bone marrow , adipogenesis , osteoblast , bone remodeling , chemistry , mesenchymal stem cell , osteoporosis , stromal cell , adipose tissue , microbiology and biotechnology , biology , neuropeptide , receptor , in vitro , biochemistry
A differentiation switch of bone marrow mesenchymal stem/stromal cells (BMSCs) from osteoblasts to adipocytes contributes to age‐ and menopause‐associated bone loss and marrow adiposity. Here it is found that osteocytes, the most abundant bone cells, promote adipogenesis and inhibit osteogenesis of BMSCs by secreting neuropeptide Y (NPY), whose expression increases with aging and osteoporosis. Deletion of NPY in osteocytes generates a high bone mass phenotype, and attenuates aging‐ and ovariectomy (OVX)‐induced bone‐fat imbalance in mice. Osteocyte NPY production is under the control of autonomic nervous system (ANS) and osteocyte NPY deletion blocks the ANS‐induced regulation of BMSC fate and bone‐fat balance. γ ‐Oryzanol, a clinically used ANS regulator, significantly increases bone formation and reverses aging‐ and OVX‐induced osteocyte NPY overproduction and marrow adiposity in control mice, but not in mice lacking osteocyte NPY. The study suggests a new mode of neuronal control of bone metabolism through the ANS‐induced regulation of osteocyte NPY.